2020
DOI: 10.1161/circresaha.119.316159
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Reactive Oxygen-Forming Nox5 Links Vascular Smooth Muscle Cell Phenotypic Switching and Extracellular Vesicle-Mediated Vascular Calcification

Abstract: Rationale: Vascular calcification, the formation of calcium phosphate crystals in the vessel wall, is mediated by vascular smooth muscle cells (VSMCs). However, the underlying molecular mechanisms remain elusive precluding mechanism-based therapies. Objective: Phenotypic switching denotes a loss of contractile proteins and an increase in migration and proliferation, whereby VSMCs are termed synthetic. We examined how VSMC phenotypic switching influences… Show more

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Cited by 123 publications
(100 citation statements)
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References 71 publications
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“…VMSC osteogenic switch occurs in both medial and atherosclerotic vascular calcification (41). RNA-Seq analysis revealed that the JAK/STAT and PPAR signaling pathways are involved in both medial and atherosclerotic calcification.…”
Section: Discussionmentioning
confidence: 99%
“…VMSC osteogenic switch occurs in both medial and atherosclerotic vascular calcification (41). RNA-Seq analysis revealed that the JAK/STAT and PPAR signaling pathways are involved in both medial and atherosclerotic calcification.…”
Section: Discussionmentioning
confidence: 99%
“…Matrix vesicles are extracellular vesicles with a high Ca 2+ content which play a role in vascular calcification [ 91 ]. Recently, the role of Nox-5 has been uncovered in Ca 2+ and matrix vesicle-induced vascular calcification [ 92 ]. In response to high extracellular Ca 2+ , VSMCs undergo a phenotype switch from a contractile to a synthetic phenotype, which is associated with increased ROS production and increased Nox-5 activity [ 92 ].…”
Section: The Involvement Of Ros In Vascular Calcificationmentioning
confidence: 99%
“…Recently, the role of Nox-5 has been uncovered in Ca 2+ and matrix vesicle-induced vascular calcification [ 92 ]. In response to high extracellular Ca 2+ , VSMCs undergo a phenotype switch from a contractile to a synthetic phenotype, which is associated with increased ROS production and increased Nox-5 activity [ 92 ]. Modulation of Nox-5 expression itself regulates phenotypic marker expression of VSMCs; namely, Nox-5 overexpression decreases the levels of contractile markers, while decreased Nox-5 expression is associated with higher expression of contractile markers and reduced calcification potential [ 92 ].…”
Section: The Involvement Of Ros In Vascular Calcificationmentioning
confidence: 99%
“…Numerous studies have documented increased thickness of smooth muscle layers and media-to-lumen ratio of arteries in hypertension,68,80,81 which may be the result of maladaptive alterations in VSMCs and the components of the adventitia 82,83. EVs are involved in the thickening of vascular smooth muscle layers and altering of components of the adventitia by different mechanisms that may be related to their different cellular origins 8489. For example, platelet-derived EVs exert a strong immunomodulatory activity by increasing monocyte adhesion to VSMCs and interacting with increased CD40- and P-selectin, inducing a switch towards a pro-inflammatory phenotype, stimulating VSMC proliferation and migration 89.…”
Section: Mechanisms Of Ev-mediated Regulation Of Blood Pressurementioning
confidence: 99%